IL-10 and TNF<b>α</b>Genotypes in SLE

López, Patricia; Gutiérrez, Carmen; Suárez, Ana

doi:10.1155/2010/838390

Cited by 50 publications

(42 citation statements)

References 101 publications

(109 reference statements)

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“…IL-10 genetic variants are associated with higher IL-10 production (Turner et al, 1997;Suarez et al, 2003;López et al, 2010;Sofian et al, 2013). Sofian et al (2013) reported that IL-10 promoter polymorphisms were not associated with HBV infection, and the A/A genotype at position -592 and the T/T genotype at position -819 were more frequently observed in patients with HBV.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-10 gene promoter polymorphism and risk of liver cirrhosis

Liu

Zhang

et al. 2015

Genet. Mol. Res.

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ABSTRACT. We conducted a hospital-based case-control study to assess the association between IL-10-592 A/C, IL-10-819 C/T, and IL-10-1082 A/G polymorphisms and the risk of liver cirrhosis in a Chinese population. This 1:1-matched case-control study included 192 patients from the Chinese PLA General Hospital. Genotypes of IL-10-592 A/C, IL-10-819 C/T, and IL-10-1082 A/G were detected by polymerase chain reaction amplification-restriction fragment length polymorphism analysis. Conditional regression analysis showed that individuals carrying the IL-10-1082 G allele had an only slightly increased risk of liver cirrhosis, with an adjusted odds ratio (95% confidence interval) of 2.14 (0.97-1.68). However, we did not identify a significant association between polymorphisms in IL-10-592 A/C and IL-10-819 C/T and the risk of liver cirrhosis. These findings may provide important clues for future studies of early detection screening of liver cirrhosis.

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Section: Discussionmentioning

confidence: 99%

Interleukin-10 gene promoter polymorphism and risk of liver cirrhosis

Liu

Zhang

et al. 2015

Genet. Mol. Res.

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“…In humans, the amount of IL-10 production after insults is genetically determined and polymorphic at position of –1082 (rs1800896). However, the effects of genetic element mosaics in IL-10 can vary for different inducing agents [24], and there are remarkable differences in the distribution of IL-10 genotypes between Han Chinese and other populations [25]. Although the IL-10 tissue levels after CM exposure cannot be obtained, the low serum levels before CM exposure and the different IL-10 (rs1800896) SNP distributions in CIN patients, both provide useful evidence that IL-10 plays an important role in this condition and that changing IL-10 levels may modify CIN pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

“…Our study enhances the understanding of the pathogenesis, identifying potential markers of susceptibility, severity and clinical renal outcomes in patients after PCI. Third, although a growing dispute in studies of SNPs, the functional effects in the selected TNF-α and IL-10 SNPs were well studied [6,24,25]. The biological plausibility was established between CIN and TNF-α/IL-10.…”

Section: Discussionmentioning

confidence: 99%

Gene Polymorphisms of Interleukin-10 and Tumor Necrosis Factor-α Are Associated with Contrast-Induced Nephropathy

Chang

Yang

et al. 2013

Am J Nephrol

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Background/Aims: Contrast-induced nephropathy (CIN) is the third most common cause of hospital-acquired acute renal failure. However, the pathogenesis of CIN remains unclear. This study evaluated the role of anti-inflammatory cytokine interleukin-10 (IL-10) and pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) gene polymorphisms as CIN susceptibility markers after percutaneous coronary intervention (PCI). Methods: Four IL-10 tag SNPs (rs1554286, rs3021094, rs3790622, rs1800896) and three TNF-α tag SNPs (rs1799964, rs1800630, rs1800629) were analyzed by MALDI-TOF mass spectrometry in 53 CIN patients and 455 control subjects. Serum IL-10 and TNF-α were detected using ELISA. Results: When compared to controls, the CIN patients showed increased frequencies of CC (rs1554286) and AG+GG (rs1800896) genotypes in IL-10 and GA+AA (rs1800629) genotype in TNF-α (OR = 2.24 (1.13–4.44), p = 0.018; OR = 2.61 (1.30–5.26), p = 0.005, and OR = 2.11 (1.08–4.09), p = 0.025, respectively). Baseline serum IL-10 levels in CIN patients were significantly lower (1.02 ± 1.14 vs. 2.78 ± 4.73 pg/ml, p = 0.008). Patients with CIN had a higher rate of decline in renal function than those without CIN (0.89 ± 1.67 vs. 0.30 ± 0.95 ml/min/1.73 m² per month, p = 0.002). Significantly higher rates of decline in creatinine clearance were noted in patients with TNF-α (rs1800629) GA+AA than GG genotype (0.88 ± 1.83 vs. 0.36 ± 0.70, p = 0.03), and with IL-10 (rs1800896) AG+GG than AA genotype (1.28 ± 2.14 vs. 0.33 ± 0.90, p < 0.001). Conclusions: Gene polymorphisms of IL-10 and TNF-α are associated with CIN risk and long-term renal outcome after PCI. More prospective studies are needed to confirm our results.

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“…23 However, we reached no conclusive result about its involvement in SLE susceptibility. 24 One meta-analysis study showed only an association of the IL10.G11 allele with SLE susceptibility in the populations analyzed (odds ratio ¼ 1.279; 95% confidence interval: 1.027 --1.593; P ¼ 0.028). 25 We instead noted the inverse relationship existing between DNA methylation and SLE disease activity and the high association between the hypomethylated IL10 genes and SLE (odds ratio ¼ 22.061; 95% confidence interval: 9.643 --50.473; P ¼ 0.000).…”

Section: Ingenuity Pathway Analysismentioning

confidence: 97%

A whole genome methylation analysis of systemic lupus erythematosus: hypomethylation of the IL10 and IL1R2 promoters is associated with disease activity

Lin

et al. 2011

Genes Immun

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The etiology of systemic lupus erythematosus (SLE) involves a complex interaction of genetic and environmental factors. Investigations have shown that environmentally driven epigenetic changes contribute to the etiology of SLE. Here, we hypothesize that aberrant DNA methylation may contribute to the activation of the immune machinery and trigger lupus disease activity. A whole genome methylation array was applied to investigate the DNA methylation changes between 12 pairs of active SLE patients and healthy controls. The results were further confirmed in 66 SLE patients, 102 healthy controls. The methylation statuses of the IL10 and IL1R2 genes were significantly reduced in the SLE patient samples relative to the healthy controls (age-adjusted odds ratios, 64.2 and 16.9, respectively, Po0.0001). There was a trend toward SLE patients having hypomethylated IL10 and IL1R2 genes accompanied by greater disease activity. We observed that the methylation degree of IL10 and IL1R2 genes were reduced in the rheumatoid arthritis (RA) patients as well but the hypomethylation change was more significant in IL1R2 genes than in the IL10 genes in RA patients. This study demonstrated that DNA hypomethylation might be associated with SLE. Hypomethylated IL10 and IL1R2 genes may provide potential epigenetic markers as clinical predictors for autoimmune diseases.

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IL-10 and TNFαGenotypes in SLE

Cited by 50 publications

References 101 publications

Interleukin-10 gene promoter polymorphism and risk of liver cirrhosis

Interleukin-10 gene promoter polymorphism and risk of liver cirrhosis

Gene Polymorphisms of Interleukin-10 and Tumor Necrosis Factor-α Are Associated with Contrast-Induced Nephropathy

A whole genome methylation analysis of systemic lupus erythematosus: hypomethylation of the IL10 and IL1R2 promoters is associated with disease activity

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